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Hypothyroidism, Hashimotos & Iodine

It has been known for many years that a lack of iodine can create a goiter. What is a goiter you ask? A goiter is the swelling of the thyroid gland in an attempt to capture more iodine from the blood stream in a deficient state. Goiter is more common in 3rd world countries where overall nutrition is lacking. We saw it in the United States prior to the addition of iodized salt into the American diet. The image below represents a goiter in a child. The next image is a severe case. The fear of iodine has instituted the reemergence of goiter in our modern society. Look around you. You will begin to see it especially in women.

The picture below is me in 1999 when my son (my first) was born. No one noticed the nodule on my neck combined with the goiter. It turned into thyroid cancer. I believe it could have been avoided.

Supplementation with iodine will work to eliminate goiters. But what about other thyroid conditions? In this blog we will consider hypothyroidism, hashimotos, and thyroid cancer. Hyperthyroidism and graves will be covered in a future blog. These diseases all share a common issue – Iodine deficiency – while the symptoms manifest in different ways.

Hypothyroidism is defined as the body’s inability to produce sufficient thyroid hormones. The hypothalamus creates thyrotropin releasing hormone (TRH) which acts upon the pituitary gland to regulate the release of TSH (Thyroid Stimulating Hormone). Thyroid hormone creation is stimulated by the TSH action on the thyroid gland. The pituitary gland bombards the thyroid with this hormone when it gets behind telling it to make more. The higher the TSH lab number the more there is an indication that it is screaming at the gland “I NEED HORMONES NOW”. The TSH hormone also stimulates the Sodium Iodine Symporters (NIS) to take in iodine when the follicular cells “see” it pass by in the blood. Once inside the thyroid cell, the iodine is acted upon by several chemical processes and is bound to tyrosine and thyroglobulin to form Thyroxine (T4) and Tri-iodothyronine (T3). The thyroid gland creates 20% of the T3 directly in the thyroid gland. The remaining 80% is converted from T4 in the liver and kidneys. T3 is the active metabolic hormone. If iodine is not supplied in sufficient amounts, then hormone levels fall and the entire body spirals into illness.

Another complication to hypothyroidism is an autoimmune form called Hashimotos which was named for Dr Hashimoto in Japan, who discovered the disease. Hashimotos is diagnosed by lab tests measuring thyroid peroxidase antibodies (TPO Ab) and thyroglobulin antibodies (Tg Ab). The first antibody, TPO, is an attack against the oxidation process where iodine is converted to iodide and bound to the proteins for hormone creation. The Tg Ab is an attack on the thyroglobulin protein. Both hormone synthesis processes can be seen in the diagram below.

Why does the body create antibodies? For more information on why the body attacks itself in an autoimmune disease please visit this page from the NIH. Basically it is a sign that something has gone wrong and is out of balance. Many things can contribute to autoimmune thyroid disease (AIT). One of the key elements is a lack of iodine.

When the oxidation process occurs in the follicle colloid, hydrogen peroxide acts upon iodine to change it to iodide which is when it iodinates the proteins. When iodine is missing the body attempts to make thyroid hormones but the main component is missing. It is believed that in a deficient state the oxidation continues out of control which causes inflammation and damage to the cells. The body views the cells as an invader because they are not normal and creates antibodies to attack it. The key to combating this is in iodine supplementation. When supplied in amounts 100x the RDA (.150 mgs) or more, iodolipids are created which is the control mechanism on the oxidation process in the cells. The increase iodine level not only allows for hormone creation but also iodolipid creation. What the exact value in milligrams is to create this “brake” reaction is not definable. There are too many variables for each individual to predict. At this point it is a matter of trial followed by laboratory testing to determine the appropriate amount. The diagram below shows iodine entering the cell and then combining with Tg and being acted upon by TPO.

Now lets assume that Hashimotos goes undetected or untreated and no iodine is supplied. The thyroid struggles and struggles to keep up. The person must keep moving so the body now draws off of the adrenals to pick up the slack. But the adrenals are the sprinters and not the marathon runners and they will eventually crash and burn resulting in complete adrenal fatigue. These glands also need iodine and since the thyroid is grabbing all it can they are left deficient too.

Inside the thyroid gland, the TPO, Tg or both types of antibodies are attacking the gland. This results in more and more damage that can develop into nodules on the gland. At first they can be benign in nature but eventually they run the risk of becoming malignant in the form of thyroid cancer. There are several forms of thyroid cancer; Papillary, Follicular, and Medullary being the most common. Papillary and Follicular are treated using radioactive iodine (RAI) because the cancer cells will take up the iodine and be killed. Medullary thyroid cancer originates in the “C” cells of the thyroid which is where calcitonin is created. This form of thyroid cancer seems to be unrelated to iodine status although the maintenance of normal cell structure is part of iodine’s “job” in the body so it may play a role.

I mentioned in passing that RAI was used for the treatment of papillary and follicular thyroid cancer. It is used because the goal of the treatment is to kill off any remaining thyroid and cancer cells after a total thyroidectomy. They then use the Tg levels to monitor if there is cancer or not (assuming that RAI killed all the cells off) because only these cells create the Tg protein. This is great in concept if the cells do, in fact, take up the radioactive iodine. In my case they did not. I had 0.2 and 0.3% uptake in my scans. My doctors reaction each time was to get a bigger stick. I went from 100 mCi’s to 150 mCi’s and then finally 250 mCi’s in an attempt to beat the cells into submission (aka death) after 3 recurrences. It did not work. Endocrinologists call this “iodine resistance”. I believed my case was hopeless…… but then I met Dr David Brownstein.

The testing Dr Brownstein did on me may have revealed the reason for this resistance. It was a component that the majority of thyroid disease sufferers are also afflicted with. It’s bromide poisoning. When the body is deficient in iodine it attempts to find the next closest halide to replace it. Most of us are toxic in this halide so our receptors are being blocked by bromide which stops what little iodine that enters the blood stream from being taken into the cells until very large amounts of iodine are supplied. In my case it took 125 mgs which resulted in 66 mgs / L (toxic = >5 mgs / L) of bromide being release during my 24 hour Iodine Loading test. We’ll talk about testing in a future post so don’t panic. I believe that my high toxicity stopped all RAI treatments from working to kill the cells. Now combine that with the low iodine diets I was forced to do for 6 weeks prior to treatment and then never supplementing to put it back in and you have a recipe for disaster. The reason I say this is because iodine is needed for the P53 gene. This gene is called the Keeper of the Genetic Code. It is needed in the process known as apoptosis (programmed cell death) that occurs when a cell becomes abnormal. So I was toxic, radiating my body and depleting it of a much needed whole body nutrient. I believe this was why my cancer kept returning – each time stronger. It was non-radioactive iodine that was a key component in eliminating my thyroid cancer in 3 years.

Hopefully you can now see why iodine is important in managing thyroid disease.